Edward H. Koo

The paper investigates how caspase cleavage of APP contributes to Aβ-induced synaptic dysfunction and spine loss in neurons.

The paper investigates dimerization of APP family members in cultured cells and mouse brains, finding higher dimerization in brain tissue and enrichment in synaptic compartments, with reduced dimers in AD patients.

This study shows that localized APP pathology in hippocampal CA3 cells leads to altered neuronal firing patterns in connected regions, suggesting disease progression can occur through physiological dysfunction rather than just spreading pathology.

This study shows that Aβ-induced synaptic injury in hippocampal neurons is mediated by presynaptic APP expression, as demonstrated by orientation-specific LTP reduction and synaptic loss.

The paper identifies proteome-wide changes in mouse models of Alzheimer's disease, highlighting ApoE dysregulation and synaptic protein loss.